Spontaneous preterm labour remains a major obstetric problem because of the high incidence of neonatal mortality or long-term handicap associated with it. The drugs available for the management of preterm labour are poorly effective and have potentially serious side-effects for the mother or fetus. In recent years, there has been a remarkable increase in the knowledge of the biochemical mechanism underlying uterine quiescence and contractility. Many of the G protein-coupled receptors that participate in the regulation of myometrial activity have been cloned and characterized, and their intracellular signalling pathways have been elucidated. The role of G protein receptor kinases in uterine tachyphylaxis is better understood. New developments in our understanding of the cellular mechanisms involved in uterine contractions in idiopathic and infection-associated preterm labour are expected, which will lead to better, more selective therapy for this problem. However, much research remains to be done before the mechanism of human parturition is fully understood.